Invasive hemodynamic evaluation of sublingual captopril and nifedipine in patients with arterial hypertension after abdominal aortic surgery
- PMID: 7736741
- DOI: 10.1097/00003246-199505000-00011
Invasive hemodynamic evaluation of sublingual captopril and nifedipine in patients with arterial hypertension after abdominal aortic surgery
Abstract
Objectives: To examine the central hemodynamic and blood gas responses to sublingual captopril and nifedipine administration in patients with arterial hypertension after abdominal aortic surgery.
Design: Prospective, randomized, parallel-group clinical study.
Setting: Twenty-nine-bed medical-surgical intensive care unit in a university hospital.
Patients: Twenty patients with arterial hypertension (mean arterial pressure of > or = 115 mm Hg) the day after abdominal aortic surgery. Patients with bilateral renal artery stenoses, identified with the preoperative angiogram, were excluded.
Interventions: Pressures were measured using intravascular catheters and cardiac output was determined by thermodilution for 2 hrs after captopril 25 mg (n = 10) or nifedipine 10 mg (n = 10) was administered by the sublingual route.
Measurements and main results: Captopril administration and nifedipine administration decreased mean arterial pressure (from 121 +/- 1 to 94 +/- 4 mm Hg and from 121 +/- 2 to 94 +/- 2 [sem] mm Hg, respectively), pulmonary arterial pressure, pulmonary artery occlusion pressure, and right atrial pressure (p < .001 for all variables). Changes in heart rate and in cardiac output were not significant. PaO2 decreased after nifedipine, from 101 +/- 8 to 81 +/- 3 torr [13.5 +/- 1.1 to 10.8 +/- 0.4 kPa] (p < .01), but not after captopril (104 +/- 9 to 100 +/- 7 torr [13.9 +/- 1.2 to 13.3 +/- 0.9 kPa]). Excessive or symptomatic decreases in blood pressure were not observed, nor was deterioration in renal function observed.
Conclusions: Sublingual captopril and nifedipine were equally effective for the treatment of arterial hypertension after abdominal aortic surgery. Nifedipine, but not captopril, caused a deterioration in pulmonary gas exchange.
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